2 Flashcards

1
Q

What two main groups of antibiotics inhibit cell wall synthesis

A

Beta lactams

Glycopeptide

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2
Q

Name the three subgroups of beta lactams

A

Penicillins
Cephalosporins
carbapenems

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3
Q

Between pen v and pen g which is better orally absorbed

A

Penicillin v

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4
Q

Which beta lactam is good against staphylococci

A

Flucloxacillin

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5
Q

Give two examples of cephalosporins

A

Cefalexin

Ceftazidime

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6
Q

Name two examples of carbapenems and what they do

A

Ertapenem- orally absorbed

Meropenem - very broad spectrum

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7
Q

Mode of action of beta lactams

A

Block active site of penicillin binding protein and stops cross linking between cell wall components therefore is susceptible to osmotic lysis

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8
Q

What are beta lactams often given in combination with and why

A

Beta lactamase inhibitors because many bacteria produce beta lactamases that hydrolyse the beta lactam ring and inactivate it

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9
Q

Give an example of a beta lactamase inhibitor and an example of a well known combination

A

Clavulanic acid

Co-amoxiclav (amoxicillin and clavulanic acid)

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10
Q

What is the mode of action of glycopeptide antibiotics

A

Block the binding site of the penicillin binding protein and stop cell wall cross-linking

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11
Q

Give two examples of glycopeptide antibiotics

A

Vancomycin

Teicoplanin

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12
Q

Name some bacteria that glycopeptides are useful for due to beta lactam resistance

A

MRSA
Coagulase negative staphylococci
Penicillin resistance entercocci and streptococci
Clostridium difficile

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13
Q

Name the three groups of protein synthesis inhibitors

A
Macrolides 
Tetracyclines 
Aminoglycosides 
Rifamycins
Lincosamides
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14
Q

Give two examples of macrolides

A

Erythromycin

Clarithromycin- community acquired pneumonia (legionella and mycoplasma)

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15
Q

Give examples of tetracyclines

When you use them and when you don’t

A

doxycycline and tigecycline
Broad spectrum.
Not in pregnancy children or in neutropenia ( bacteriostatic)

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16
Q

Give examples of aminoglycosides

Why do you have to be careful with them

A

Gentamicin- sepsis
Amikacin
Tobramycin - anti-pseudomonal in CF

Narrow therapeutic window

17
Q

How do protein synthesis inhibitors work?

A

Inhibit either the 30s subunit ( aminoglycosides, tetracyclines)
50s (macrolides, chloramphenicol)
Or mRNA ( rifamycins)

18
Q

Name two modes of DNA synthesis/replication inhibitors

A

Nucleotide synthesis- folate inhibition

DNA gyrase inhibition- stop unwinding for replication

19
Q

Name three groups of DNAsyn/rep inhibitors

A

Sulphonamides- folate synthesis inhibitors
Diaminopyrimidines- folate synthesis inhibitors
Quinolones- additions of fluorine atom - fluoroquinolones

20
Q

What are the groups of fungi

A

Yeasts, molds and diamorphic

21
Q

Give examples of mycosis

A

Tinea ( ringworm)
Candidiasis
Mucormycosis
Aspergillosis

22
Q

What are the three main groups of antifungal drugs

A

Azoles
Polyenes
Echinocandins

23
Q

How do triazoles act

Give examples of them

A

Inhibit ergosterol synthesis (fungal alternative to cholesterol of cell membrane)
Fluconazole

24
Q

How do Polyenes act

Give examples

A

Bind ergosterol

Amphotericin B
Nystatin

25
Q

How do Echinocandins act

give examples

A

Inhibit glucan ( cell wall)
Caspofungin
Micafungin

26
Q

Name all the modes of antibiotic action

A

Inhibits cell wall synthesis
Inhibits protein synthesis
Interferes with DNA synthesis and replication
Disrupts cell membrane

27
Q

How is acyclovir selective

A

Only activated in infected cells
Becomes concentrated in infected cells due to gradient
Higher affinity for viral DNA polymerase then cellular enzymes